Lung clearance, translocation, and acute toxicity of arsenic, beryllium, cadmium, cobalt, lead, selenium, vanadium, and ytterbium oxides following deposition in rat lung

Rhoads, K.; Sanders, C.L.

doi:10.1016/0013-9351(85)90031-3

Cited by 94 publications

(48 citation statements)

References 23 publications

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“…Low urinary concentration for BeO-F was in accordance with other animal studies which have demonstrated very slow pulmonary clearance for this species (Sanders et al, 1975;Rhoads and Sanders, 1985). It is usually reported that the retention of Be in the lung can play an important role in the development of lung infl ammation (Salehi et al, 2009), but this is not obvious in our study.…”

Section: −1supporting

confidence: 92%

“…The primary routes of Be are urine and feces. In rats and dogs, wholebody clearance of inhaled Be follows a single-phase exponential curve with a half-life of 300-400 days (Finch et al, 1990;Rhoads and Sanders, 1985). Absorbed Be is generally eliminated primarily in the urine (Stiefel et al, 1980), whereas excretion of unabsorbed Be is primarily via the fecal route shortly after mucociliary clearance from the respiratory tract (Finch et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

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Urinary levels, tissue concentrations and lung inflammation after nose‐only exposure to three different chemical forms of beryllium

Müller¹,

Mazer²,

Salehi³

et al. 2010

J of Applied Toxicology

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This study aimed to determine the toxicity and toxicokinetic of three Be chemical species A total of 120 mice (four groups of 30) were nose-only exposed. The first group was used as a control while the three others were exposed to 250 microg m(-3) of fine particles of three different Be species (Be metal, Be-F; Be oxide, BeO-F; Be aluminium, BeAl-F). Exposure lasted over three consecutive weeks, five days per week and 6 h per day. Blood and several tissues were collected one week after exposure. Urines were collected before the beginning of exposure, at the end of every week of exposure and one week after exposure. Results showed that urine concentrations were different from one Be species to another and that excretion continued after the end of exposure. Except for BeO-F, where Be urine concentrations were stable during the three weeks of exposure, concentrations of Be-F and BeAl-F reached a peak after the first week. According to particle size, BeO-F obtained the highest theoretical pulmonary deposition rate, which partially led to the highest Be lung concentration. This group also presented the lowest urine concentration but that did not lead to more severe lung inflammation. Moreover, even if BeAl-F obtained the lowest percentage theoretical pulmonary deposition, it showed the highest Be urinary concentration, the lowest Be lung concentration and the lowest lung toxicity. In this specific case, a high Be concentration in urine did not reflect a high exposure or a severe toxic effect.

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Section: −1supporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Urinary levels, tissue concentrations and lung inflammation after nose‐only exposure to three different chemical forms of beryllium

Müller¹,

Mazer²,

Salehi³

et al. 2010

J of Applied Toxicology

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show abstract

“…Rhoads and Sanders (51) have reported a half-time of intratracheally instilled Yb2O3 in the rat lung of 21 days. In these intratracheal instillation studies, translocation of RE to extrapulmonary tissue was marginal or below the detection limit.…”

Section: Exposure To Rare Earthsmentioning

confidence: 98%

Exposure, Metabolism, and Toxicity of Rare Earths and Related Compounds

Hirano¹,

Suzuki²

1996

Environmental Health Perspectives

152

187

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“…In rats, females exhibited less efficient clearance and earlier morbidity and mortality from exposure. 35 Rhoades and Sanders 36 reported a 400 day half life for clearance of beryllium oxide from rat lung. In a dose study of beryllium sensitization and chronic beryllium disease in a beryllium machining plant, 20 of 235 individuals who had lifetime weighted average airborne exposures between 0.024 μg/m 3 and 0.6 μg/m 3 , well below the 2 μg/m 3 occupational exposure limit intended to prevent chronic beryllium disease, nevertheless were found to be sensitized to beryllium.…”

Section: Berylliummentioning

confidence: 99%

Toxic elements in tobacco and in cigarette smoke: inflammation and sensitization

2011

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Biochemically and pathologically, there is strong evidence for both atopic and nonatopic airway sensitization, hyperresponsiveness, and inflammation as a consequence of exposure to tobacco mainstream or sidestream smoke particulate. There is growing evidence for the relation between exposure to mainstream and sidestream smoke and diseases resulting from reactive oxidant challenge and inflammation directly as a consequence of the combined activity of neutrophils, macrophages, dendritic cells, eosinophils, basophils, as a humoral immunological consequence of sensitization, and that the metal components of the particulate play a role in adjuvant effects. As an end consequence, carcinogenicity is a known outcome of chronic inflammation.Smokeless tobacco has been evaluated by the IARC as a group 1 carcinogen. Of the many harmful constituents in smokeless tobacco, oral tissue metallothionein gradients suggest that metals contribute to the toxicity from smokeless tobacco use and possibly sensitization.This work reviews and examines work on probable contributions of toxic metals from tobacco and smoke to pathology observed as a consequence of smoking and the use of smokeless tobacco. Metals and metalloids in tobaccoThough exposure to substances from tobacco use is obviously a complex exposure, the carcinogens in tobacco smoke have been classified for health risk determinations into five major chemical classes. 1 Some of these have been carefully studied, contributing to a strong weight of evidence for associated health risks. 2 Toxic metals and metalloids constitute one of the more understudied major carcinogenic chemical classes in smokeless tobacco products and tobacco smoke. Eight of the top forty substances in the Fowles and Dybing table of cancer risk indices are metals or metalloid compounds. 1 In their table of non-cancer risk indices for individual chemical constituents of mainstream cigarette smoke based on a single cigarette per day, three of the top eight listed for respiratory effect health risk, cadmium, hexavalent chromium, and nickel, were metals. Another metalloid, silicon in the form of silicates, poses serious health risks by inhalation, but limited data is available, likely due to analytical difficulties.Metals and metalloids in smoke from biomass combustion including tobacco are generally considered to be present in ionic form, but may also occur in a gaseous elemental form, as is the case for mercury. 3 Whether a tobacco product is consumed by smoking or in a smokeless form, the exposure to toxic metals is directly related to the concentration in the tobacco leaf, assuming no metal containing additives are included during manufacture. [4][5][6] The soil (including any amendments to the soil such as sludge, fertilizers, or irrigation with

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Lung clearance, translocation, and acute toxicity of arsenic, beryllium, cadmium, cobalt, lead, selenium, vanadium, and ytterbium oxides following deposition in rat lung

Cited by 94 publications

References 23 publications

Urinary levels, tissue concentrations and lung inflammation after nose‐only exposure to three different chemical forms of beryllium

Urinary levels, tissue concentrations and lung inflammation after nose‐only exposure to three different chemical forms of beryllium

Exposure, Metabolism, and Toxicity of Rare Earths and Related Compounds

Toxic elements in tobacco and in cigarette smoke: inflammation and sensitization

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